ライフサイエンスコーパス: IPMN

1 IPMN recurrences and deaths from cancer occurred in pati

2 IPMN type and main pancreatic duct diameter were signifi

3 IPMNs involving the MPD harbor a high likelihood of mali

4 IPMNs of the pancreas are estimated to have a better pro

5 IPMNs represent an increasing indication for pancreatic

6 alysis, NLR value higher than 4 (P < 0.001), IPMN cyst of size more than 3 cm (P < 0.001), presence o

7 FI: IPMN 11.4, MCN 13.0, SCA 5.3; P < 0.001, IPMN vs. SCA) and CA72.4 (median FI: IPMN 10.4, MCN 10.5

8 FI: IPMN 10.4, MCN 10.5, SCA 9.9; P = 0.003, IPMN vs. SCA).

9 Ten of 13 IPMNs with moderate dysplasia or malignancy had loss of

10 overy set of 18 surgical samples (11 PDAC, 4 IPMN, 3 C).

11 rom the corresponding surgical specimens, 57 IPMNs were separated and subdivided by histologic criter

12 Set 1-52 surgical samples (24 PDAC, 7 IPMN, 6 chronic pancreatitis, 15 C), and set 2-95 endosc

13 d-guided fine-needle aspirations (60 PDAC, 9 IPMN, 26 C).

14 isplayed detectable chromosomal aberrations, IPMNs with moderate and high-grade dysplasia showed freq

15 f life-long follow-up after resection for an IPMN.

16 ndent risk factors for the development of an IPMN with HGD or an invasive carcinoma in the remnant pa

17 A, invasive adenocarcinoma arising within an IPMN was associated with a lower incidence of (1) advanc

18 biologic and clinical behavior of IPMNs and IPMN-associated adenocarcinomas is different from PDAC i

19 miRNome analysis shows that PDAC and IPMN have differential miRNA profiles with respect to C,

20 ssion is significantly increased in PDAC and IPMN lesions.

21 s were significantly deregulated in PDAC and IPMN versus C.

22 RNAs commonly overexpressed in both PDAC and IPMN were selected for further validation.

23 on (P < 0.05) was identified between SCA and IPMN (34/51 proteins, 67%) and between SCA and MCN (13/5

24 tein expression was observed between SCA and IPMN for the majority of proteins assessed and multimark

25 ion accurately discriminated between SCA and IPMN in 92% of patients.

26 demonstrated distinct clustering of SCA and IPMN with some cross-over between MCN.

27 overall accuracy rate of 92% between SCA and IPMN.

28 SPNs are low-grade malignancies, and IPMNs and MCNs, but not SCAs, have the capacity to progr

29 intraductal papillary mucinous neoplasm (BD IPMN; 67%), whereas also being specific (85 and 88%, res

30 in mucinous cysts, particularly in small BD IPMN.

31 ohort was 68 years, 56% had branch duct (BD)-IPMN and 21% had invasive cancers.

32 BD-IPMN patients are at risk of pancreatic carcinogenesis.

33 eatic and extrapancreatic malignancies in BD-IPMN patients.

34 Invasive cancer arising in BD-IPMN was found in 23 patients of the entire cohort (4%),

35 y about surgery of branch-duct type IPMN (BD-IPMN).

36 than 3 cm and in 25% of "Sendai-negative" BD-IPMN.

37 Recurrence of noninvasive BD-IPMN is infrequent and surveillance may be avoided in se

38 Expectant management of BD-IPMN following the old guidelines is safe, whereas cauti

39 carcinoma or carcinoma in situ in 67% of BD-IPMN smaller than 3 cm and in 25% of "Sendai-negative" B

40 The diagnosis of BD-IPMN was based on the presence of unilocular or multiloc

41 head cyst radiographically suggestive of BD-IPMN, including the following: (1) initial pancreaticodu

42 d worrisome features in the management of BD-IPMN.

43 m 577 patients with suspected or presumed BD-IPMN under surveillance at the Massachusetts General Hos

44 o the revised guidelines, 76% of resected BD-IPMN with carcinoma in situ and 95% of resected BD-IPMN

45 ith carcinoma in situ and 95% of resected BD-IPMN with invasive cancer had high-risk stigmata or worr

46 In 33 patients (9%), a residual BD-IPMN was left in the pancreatic remnant, but none of the

47 , 205 mixed-type (40%), and 233 suspected BD-IPMN (46%).

48 No patient developed unresectable BD-IPMN carcinoma during follow-up.

49 Patients with BD-IPMN are not at risk of extrapancreatic carcinogenesis.

50 ive database identified 563 patients with BD-IPMN.

51 imaging, many IPMNs are misclassified as BD-IPMNs but reveal mixed-type lesions in histopathology.

52 s are not sufficient to reliably diagnose BD-IPMNs, surgical resection for suspected small branch-duc

53 Of 141 Sendai negative BD-IPMNs, a malignancy rate of 18% (high-grade dysplasia an

54 intraductal papillary mucinous neoplasms (BD-IPMNs), remain uncertain.

55 intraductal papillary mucinous neoplasms (BD-IPMNs).

56 alignancy and define a subset of low-risk BD-IPMNs.

57 Most interesting, 29% of suspected BD-IPMNs (67/233) revealed histological involvement of the

58 tcomes of a large cohort of patients with BD-IPMNs to determine risk of malignancy and define a subse

59 a retrospective analysis of patients with BD-IPMNs under surveillance, their overall risk of malignan

60 ardized incidence ratio for patients with BD-IPMNs without worrisome features of malignancy at 5 year

61 rant surgical removal from 'indolent/benign' IPMNs that can be observed.

62 vocally establish it as a suppressor of both IPMNs and MCNs.

63 ails of IPMN, including communication of BPD IPMN with MPD, that are almost equivalent to those provi

64 20 and 21 of 24 branch pancreatic duct (BPD) IPMNs with CT and MRCP, respectively.

65 pancreatitis, 13 with low-grade side-branch IPMNs, and 15 patients with PDAC; histologically normal

66 cins and have characteristics of side-branch IPMNs.

67 IPMN with an associated invasive carcinoma (IPMN-INV).

68 s the first to use array CGH to characterize IPMNs.

69 t a resection for PDAC and had a concomitant IPMN.

70 efinitive pathological examination confirmed IPMN diagnosis in 95% of patients (n = 77), all except 2

71 gical resection for histologically confirmed IPMN from January 1997 to July 2015.

72 ma from a cohort of pathologically-confirmed IPMN cases of various grades of severity and non-disease

73 (G12D);Pten(DeltaDuct/+) mice, 70% developed IPMN, predominately of the pancreatobiliary subtype, and

74 Pten(DeltaDuct/DeltaDuct) mice developed IPMNs of several subtypes.

75 RNAs (GAS5 and SRA) aided in differentiating IPMNs from controls.

76 cal features that are similar to branch duct IPMN.

77 d patients with Fukuoka-negative branch-duct IPMN or pancreatic cancer.

78 al resection for suspected small branch-duct IPMN should be considered in patients fit for surgery.

79 ents with main-duct IPMN and for branch-duct IPMN with mural nodularity or positive cytology irrespec

80 ht loss, interval (from isolated branch-duct IPMN) to MPD involvement, diffuse MPD dilation, increase

81 3%), and arose in the setting of a main duct IPMN (96%).

82 idelines, which include redefining main duct IPMN and removing the recommendation for surgical resect

83 ed-type IPMN, and 82 patients with main-duct IPMN alone.

84 recommended for fit patients with main-duct IPMN and for branch-duct IPMN with mural nodularity or p

85 N) recommend surgical treatment in main-duct IPMN patients with a main pancreatic duct (MPD) diameter

86 ience of 2 tertiary centers with branch-duct IPMNs aiming to validate these recommendations.

87 Although many branch-duct IPMNs are small and asymptomatic, they harbor a signific

88 ected, pathologically confirmed, branch-duct IPMNs between 1990 and 2005 was conducted.

89 who were surgically resected for branch-duct IPMNs between January 2004 and July 2010 at the Universi

90 the current Sendai criteria for branch-duct IPMNs need to be adjusted.

91 believe that both main-duct and branch-duct IPMNs represent premalignant lesions.

92 This large cohort of resected branch-duct IPMNs shows that cancer is present in 22% of cases and v

93 onsecutively resected IPMNs, 123 branch-duct IPMNs were identified analyzing preoperative imaging.

94 Some 69 branch-duct IPMNs were less than 3 cm in size, without mural nodules

95 ar disease-specific survival for branch-duct IPMNs with noninvasive neoplasms was 100% and, for invas

96 Of all the Sendai negative branch-duct IPMNs, 24.6% (17/69) showed malignant features (invasive

97 Main-duct IPMNs with a MPD between 5 and 9 mm already bear a signi

98 tic subunit of the SWI/SNF complexes, during IPMN-PDA development.

99 Six of the eight IPMNs and three of the eight MCNs harbored mutations of

100 0.001, IPMN vs. SCA) and CA72.4 (median FI: IPMN 10.4, MCN 10.5, SCA 9.9; P = 0.003, IPMN vs. SCA).

101 nts with mucinous cysts were CEA (median FI: IPMN 11.4, MCN 13.0, SCA 5.3; P < 0.001, IPMN vs. SCA) a

102 ement of CFIMs may be a surrogate marker for IPMN progression and allow for the identification of hig

103 6, 150 patients underwent 156 operations for IPMN.

104 component and resection margin positive for IPMN were predictors of recurrence (P < 0.05).

105 otal of 223 patients underwent resection for IPMN involving the MPD.

106 Fifty-nine patients underwent resection for IPMN with an associated invasive carcinoma (IPMN-INV).

107 haracteristics, outcomes after resection for IPMN-associated and standard PDA were not significantly

108 5-year survival was 42% after resection for IPMN-associated versus 19% for standard PDA (P < 0.001).

109 avoids inappropriate standard resections for IPMN-mimicking lesions.

110 nsecutive patients who underwent surgery for IPMN between January 2004 and December 2012 were include

111 al of 605 patients who underwent surgery for IPMN, there were 320 patients with MPD involvement, 238

112 whether PDGs are a precursor compartment for IPMNs and the role of Trefoil factor family 2 (TFF2)-a p

113 All patients operated on for IPMNs between January 1, 2007, and December 31, 2012, wi

114 ic screening of 272 patients operated on for IPMNs revealed 1 patient with axial and peripheral polyo

115 from 4 high-volume centers were queried for IPMNs, with invasive components measuring 20 mm or less.

116 cells undergo "ductal retrogression" to form IPMN-PDA.

117 We aimed to identify cells that form IPMNs and mutations that promote IPMN development and pr

118 cancer at the final surgical margin, 23% had IPMN without invasive cancer at the margin, and 54% had

119 arkably, TP53INP1 is down-regulated in human IPMN.

120 metaplasia of the PDG, which resembled human IPMN; these expressed gastric mucins (MUC5AC and MUC6),

121 so observed progressive loss of p16 in human IPMNs of increasing grades.

122 In histologic analyses of human IPMNs, we found PDGs to form the basal segment and possi

123 h histologic and molecular features of human IPMNs.

124 lity as a diagnostic adjunct for identifying IPMNs and their pathology, especially when incorporated

125 surveillance so as not to overlook cancer in IPMN.

126 ncies (EPMs) occur with unusual frequency in IPMN patients.

127 Targeted-NGS on genes commonly mutated in IPMN and PDAC was performed on tumors from (1) 13 patien

128 majority of proteins were down-regulated in IPMN and MCN compared with SCA.

129 l subtypes of invasive carcinomas arising in IPMNs have been described, colloid carcinoma and tubular

130 gh-grade dysplasia and invasive carcinoma in IPMNs with MPD involvement was 68%.

131 5q, 6q, and 11q was significantly higher in IPMNs with high-grade dysplasia or invasion compared wit

132 gly associated with malignant progression in IPMNs.

133 5-year survival of patients with intestinal IPMNs was significantly better than pancreatobiliary IPM

134 Invasive IPMN recurred in 45% of cases, whereas noninvasive in on

135 antly associated with malignant and invasive IPMN (P<0.001; P<0.001).

136 s was associated with malignant and invasive IPMN (P<0.001; P<0.02).

137 In invasive IPMN recurrence depends on N status, pancreatic margin,

138 d carcinoma histological subtype of invasive IPMN had a more statistically favorable survival outcome

139 ed the regions with and without the invasive IPMN (control tissue) by immunohistochemistry.

140 mber was negatively associated with invasive IPMN (P=0.03).

141 Of the 67 invasive IPMNs, 39 were tubular carcinomas (58%) and invasion was

142 Among invasive IPMNs, the majority (58%) were mixed-type lesions accord

143 aDuct/DeltaDuct) mice all developed invasive IPMNs within 1 month.

144 recommend surgical resection of MPD-involved IPMN in fit patients.

145 As such, the natural history of MPD-involved IPMN is poorly understood.

146 Malignant IPMN was present in 32% of cases, whereas 19% of cases w

147 ter were significant predictors of malignant IPMN (P<0.001).

148 res in distinguishing 'aggressive/malignant' IPMNs that warrant surgical removal from 'indolent/benig

149 By abdominal imaging, many IPMNs are misclassified as BD-IPMNs but reveal mixed-typ

150 eoplasms (IPMNs) involving the main duct (MD IPMNs) or the main and branch ducts (mixed IPMNs) of the

151 MD-IPMN is mainly intestinal-type and malignant.

152 to preoperative imaging, 74 patients had MD-IPMN (14%), 205 mixed-type (40%), and 233 suspected BD-I

153 on has led to a redefinition of MPD IPMN (MD-IPMN).

154 Retrospective review of resected MD-IPMN from 1990 to 2013.

155 eveloped clinically significant metachronous IPMNs.

156 ents undergoing resection for an MD or mixed IPMN (59 men [57.3%]; 44 women [42.7%]; median [range] a

157 for a preoperative diagnosis of MD or mixed IPMN and in whom IPMN was confirmed by surgical patholog

158 factor for malignant disease in MD or mixed IPMN.

159 D IPMNs) or the main and branch ducts (mixed IPMNs) of the pancreatic system is a main pancreatic duc

160 ment algorithm for patients with MD or mixed IPMNs.

161 In all models, IPMNs and PDAC expressed the duct-specific lineage traci

162 r exclusion has led to a redefinition of MPD IPMN (MD-IPMN).

163 ss the clonal relationships among multifocal IPMNs.

164 ts with histologically documented multifocal IPMNs were collected and their clinicopathologic feature

165 ts with histologically documented multifocal IPMNs.

166 A majority of multifocal IPMNs (86% synchronous, 100% metachronous) were composed

167 The majority of multifocal IPMNs arise independently and exhibit a gastric-foveolar

168 In addition, thirty multifocal IPMNs arising in 13 patients from 3 hospitals were subje

169 Molecular analysis of multiple IPMNs from 13 patients demonstrated nonoverlapping KRAS

170 ived from an intestinal subtype GNAS-mutated IPMN.

171 ng intraductal papillary mucinous neoplasia (IPMN), a precursor to PDAC in humans.

172 ve intraductal papillary mucinous neoplasia (IPMN).

173 : Intraductal papillary mucinous neoplasias (IPMNs) are precancerous cystic lesions that can develop

174 of intraductal papillary mucinous neoplasm (IPMN) and mucinous cystic neoplasm were updated in 2012,

175 BD) intraductal papillary mucinous neoplasm (IPMN) espouse safety of observation of asymptomatic cyst

176 ved intraductal papillary mucinous neoplasm (IPMN) has been established by surgical series.

177 BD) intraductal papillary mucinous neoplasm (IPMN) is infrequent and that extrapancreatic malignancie

178 of intraductal papillary mucinous neoplasm (IPMN) of the pancreas.

179 and intraductal papillary mucinous neoplasm (IPMN) precursor lesions.

180 man intraductal papillary mucinous neoplasm (IPMN) specimens were analyzed by immunohistochemistry.

181 ing intraductal papillary mucinous neoplasm (IPMN) were observed as early as 2 months of age.

182 ion intraductal papillary mucinous neoplasm (IPMN), to find new microRNA (miRNA)-based biomarkers for

183 ith intraductal papillary mucinous neoplasm (IPMN).

184 ts (intraductal papillary mucinous neoplasm [IPMN], mucinous cystic neoplasm [MCN]).

185 ed intraductal papillary mucinous neoplasms (IPMN) of the pancreas with respect to risk factors of ma

186 of intraductal papillary mucinous neoplasms (IPMN) recommend surgical treatment in main-duct IPMN pat

187 ic intraductal papillary mucinous neoplasms (IPMN) using targeted next-generation sequencing (NGS).

188 4 intraductal papillary mucinous neoplasms (IPMN), 2 adenocarcinomas, 1 low-grade intraepithelial pa

189 ic intraductal papillary mucinous neoplasms (IPMN).

190 in intraductal papillary mucinous neoplasms (IPMNs) and in McCune-Albright syndrome, characterized by

191 as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological cl

192 Intraductal papillary mucinous neoplasms (IPMNs) are the most frequent cystic pancreatic tumors.

193 of intraductal papillary mucinous neoplasms (IPMNs) involving the main duct (MD IPMNs) or the main an

194 g, Intraductal Papillary Mucinous Neoplasms (IPMNs) of the pancreas are identified with increasing fr

195 Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas arising in branch ducts are thoug

196 th intraductal papillary mucinous neoplasms (IPMNs) of the pancreas.

197 ), intraductal papillary mucinous neoplasms (IPMNs), mucinous cystic neoplasms (MCNs), and solid pseu

198 ct intraductal papillary mucinous neoplasms (IPMNs).

199 ion of IPMN may include development of a new IPMN or ductal adenocarcinoma (PDAC).

200 SCA (n = 15), non main-duct and noninvasive IPMN (n = 32), and noninvasive MCN (n = 12) was aspirate

201 ients who underwent resection of noninvasive IPMN were reviewed to identify risk factors associated w

202 ected patients, PSP for presumed noninvasive IPMN in experienced hands is highly feasible and avoids

203 patients with both invasive and noninvasive IPMNs at initial resection.

204 e to differentiate invasive from noninvasive IPMNs.

205 insufficiency, and may overtreat noninvasive IPMNs.

206 ted in 91 patients with presumed noninvasive IPMNs, after complete preoperative work-up including com

207 nalysis of the 260 patients with noninvasive IPMNs showed that family history of pancreatic cancer (P

208 G cells and their overlying nonproliferative IPMN cells.

209 The favorable biologic behavior of IPMN-associated compared with standard PDA is based on i

210 detailed radiologic-based classification of IPMN type, location, distribution, size, number, cytolog

211 tients resected for an invasive component of IPMN were analyzed with detailed pathologic review of hi

212 d reformation can provide imaging details of IPMN, including communication of BPD IPMN with MPD, that

213 ergistic effects in promoting development of IPMN and progression to PDAC.

214 Evaluation of IPMN subtypes supports postoperative patient prognosis p

215 sm of neoplastic cells with the expansion of IPMN lesions in Acvr1b(flox/flox);LSL-KRAS(G12D);Pdx1-Cr

216 and histologically analyzed for formation of IPMN, pancreatic intraepithelial neoplasias, and PDAC, i

217 observed that the behavior and management of IPMN and adenocarcinoma in the pancreas graft appears co

218 r, underlining its role in the occurrence of IPMN and highlighting the importance of TP53INP1 in the

219 endent predictive marker for the presence of IPMN-associated invasive carcinoma.

220 point system for estimating the presence of IPMN-associated invasive carcinoma.

221 imply a tendency for earlier presentation of IPMN-associated invasive adenocarcinoma.

222 ve data protocol) with histological proof of IPMN who underwent surgery between January 2004 and Dece

223 atic surgery and had a histological proof of IPMN.

224 The proportion of IPMN patients having any extrapancreatic neoplasm diagno

225 the remnant pancreas following resection of IPMN may include development of a new IPMN or ductal ade

226 owever, survival outcomes after resection of IPMN-associated and after resection of standard pancreat

227 The 5-year survival after resection of IPMN-associated invasive adenocarcinoma is reported to b

228 the remnant pancreas following resection of IPMN; and (2) 10 patients who underwent a resection for

229 atients who were free of them at the time of IPMN diagnosis.

230 In Pten(DeltaDuct/DeltaDuct) mice, 31.5% of IPMNs became invasive; invasion was associated with spon

231 The biologic and clinical behavior of IPMNs and IPMN-associated adenocarcinomas is different f

232 chanisms underlying the clinical behavior of IPMNs are incompletely understood.

233 ince the authors' 2001 report, the number of IPMNs resected at our institution has more than doubled,

234 e found evidence for a ductal cell origin of IPMNs.

235 p16 (Cdkn2a) was required for progression of IPMNs to pancreatic ductal adenocarcinomas in Acvr1b(flo

236 activation on initiation and progression of IPMNs.

237 Survival following resection of IPMNs without invasive cancer (regardless of degree of d

238 ch duct types), the histological subtypes of IPMNs (ie, intestinal, pancreatobiliary, gastric, and on

239 All subtypes of IPMNs display a relevant risk for malignant transformati

240 later (P < 0.001), but patterns depended on IPMN subtypes.

241 long-term outcome particularly for oncocytic IPMNs.

242 ved between MPD diameter and clinical and/or IPMN features such as age, cyst location, mural nodules,

243 apillary mucinous neoplasms of the pancreas (IPMN) by histological subtype of the invasive component

244 tes growth of mutant KRAS-induced pancreatic IPMNs in mice; this process appears to involve NOTCH4 an

245 re mice accelerated the growth of pancreatic IPMNs compared with LSL-KRAS(G12D);Pdx1-Cre mice, but di

246 und that the invasive human pancreatobiliary IPMN tissue had lower levels of PTEN and increased level

247 a patient with an invasive pancreatobiliary IPMN and analyzed the regions with and without the invas

248 s significantly better than pancreatobiliary IPMNs (86.6% vs. 35.6%; P < 0.001).

249 165) were obtained from patients with PDAC, IPMN, or from control individuals (C), from Hospital Cli

250 , location, and distribution did not predict IPMN pathology.

251 imaging features, the accuracy of predicting IPMN pathological classification improved.

252 Patients with a primary IPMN with HGD or with positive family history are at an

253 s that form IPMNs and mutations that promote IPMN development and progression.

254 ations in GNAS have been reported to promote IPMN formation.

255 nge, 44-88 years) with pathologically proved IPMN were examined with dual-phase CT with 1.25-mm-thick

256 Recently, IPMNs have been described as a McCune-Albright syndrome-

257 were identified, comprising 25% of resected IPMN-associated carcinomas (n = 280).

258 Retrospective review of 412 resected IPMNs from 1990 to 2013 who have had near-complete follo

259 We evaluated 78 resected IPMNs (2004-2013).

260 Among a total of 287 consecutively resected IPMNs, 123 branch-duct IPMNs were identified analyzing p

261 We found that SCAs, IPMNs, MCNs, and SPNs contained 10 +/- 4.6, 27 +/- 12, 1

262 A total of 70 small IPMN-associated invasive carcinomas (</=20-mm invasion)

263 i-institutional experience of resected small IPMN-associated carcinoma.

264 atients operated on for presumptive sporadic IPMNs.

265 Synchronous IPMNs were present in 29 patients (85%), whereas 5 (15%)

266 Three synchronous IPMNs (10%) had an associated invasive cancer.

267 providing additional evidence of a syndromic IPMN as a feature of McCune-Albright syndrome, this obse

268 Benign neoplasms most frequent in the IPMN group were colonic polyps (n = 114) and Barrett's n

269 patients (17%) experienced recurrence of the IPMN, and 5- and 10-year disease-free survival (DFS) was

270 In this study, we analyzed the IPMNs from 2 pancreatic cancer referral centers by corre

271 While none of the IPMNs with low-grade dysplasia displayed detectable chro

272 One hundred ninety-three IPMN patients (38%) suffered from invasive carcinoma.

273 Patients with invasive tubular IPMN had no statistically significant difference in surv

274 of malignancy and/or invasion in branch-type IPMN.

275 ontroversy about surgery of branch-duct type IPMN (BD-IPMN).

276 lysis of human samples revealed gastric-type IPMN to comprise 2 molecularly distinct layers: a basal

277 Primary surveillance of mixed-type IPMN may be a reasonable strategy in select patients.

278 PD involvement, 238 patients with mixed-type IPMN, and 82 patients with main-duct IPMN alone.

279 urveillance, 70 for MPD-involved, mixed-type IPMN.

280 patients with asymptomatic branch-duct type IPMNs of the pancreas less than 3 cm in diameter without

281 us that main-duct (MD) as well as mixed-type IPMNs should be treated surgically due to a high risk of

282 3 most common diagnoses in the PI group were IPMN without invasive cancer (30%), cystadenoma (17%), a

283 ve diagnosis of MD or mixed IPMN and in whom IPMN was confirmed by surgical pathologic findings at a

284 ive patients were identified, 132 (10%) with IPMN-associated invasive adenocarcinoma and 1128 (90%) w

285 y, and mural nodularity were correlated with IPMN pathology.

286 d imaging data for possible correlation with IPMN-associated carcinoma in the form of a predictive no

287 All patients diagnosed with IPMN at Mayo Clinic from 1994 to 2006 were identified.

288 Patients with IPMN have increased risk of harboring extrapancreatic ne

289 re be used in the diagnosis of patients with IPMN or in monitoring disease progression.

290 lected database (1992-2012) of patients with IPMN undergoing primary surveillance was performed.

291 A total of 503 patients with IPMN underwent primary surveillance, 70 for MPD-involved

292 d GNAS mutations in cfDNA from patients with IPMN, but not in patients with serous cystadenoma or con

293 f extrapancreatic neoplasms in patients with IPMN, but these studies focused only on those patients w

294 were significantly elevated in patients with IPMN-associated invasive carcinoma (P < 0.001).

295 py should be considered in all patients with IPMN.

296 us or synchronous neoplasms in patients with IPMN.

297 Cases with IPMNs were identified, and the subtypes were distinguish

298 e some histologic and clinical features with IPMNs of the pancreas, and may represent a carcinogenesi

299 detect lncRNAs in plasma from patients with IPMNs and suggest that an lncRNA-based blood test may ha

300 resections were performed for patients with IPMNs, with 78 resections performed since January 2001.